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1950). , 1955). Most vascular areas react to the intravenous or intraarterial administration of kinins with vasodilatation which is not blocked by atropine or antihistamines. In ii1animals, kinins transiently lower both the systolic and diastolic components of the systeniic arterial pressures. 05 pg/kg is the threshold dose (Konzett and Sturiner, 1960b). Other animals also react to the administration of peptides with transient hypotension (Table 11). Pretreatment with an iiihibitor of the enzymic metabolism of kinins modifies the degree and the duration of hypotensive response considerably (Erdos and Wohler, 1963a,b).

Low concentrations of guanethidine, dibenamine, and phenoxybenzamine acted similarly on the guinea pig ileum (Rocha c Silva and Leme, 1963). Thrombin liberates two peptides during the conversion of fibrinogen to fibrin. , 1963). , 1964). It does not seem to depend on the integrity of the peptide chain or on the presence of the C-terminal arginine of peptide B. The individual amino acid components of the peptide, on the other hand, are inactive. The action of this naturally occurring peptide might be of possible physiological importance.

Herxheimer and Streseniann, 1961, 1963; Stresemann, 1963). Some of these patients reacted to the peptide with an exceptionally violent attack. 9. Interaction with Other Agents Kinins or kallikrein can act either synergistically with some other pharmacologically active agents, or they can antagonize them (Section I1,C). 8. Resistance to inflation of guinea pig lungs in vivo. Action of SRS-A and bradykinin and their antagonism by acetylsalicylic acid after pithing the spinal cord and crushing the sympathetic cervical nerves and vagi.